Eosinophils are traditionally associated with allergic and parasitic inflammation. Recently, eosinophils have also been shown to have roles in diverse processes including development, intestinal health, thymic selection, and B-cell survival with the majority of these insights being derived from murine models and in vitro assays. Despite this, tools to easily and effectively quantify tissue eosinophils without relying on surrogate markers, granule content or antibodies have been lacking. Here I used a genetically encoded eosinophil reporter mouse strain to develop and refine an image analysis toolset to accurately quantify eosinophils in tissues. Next, I applied this toolset to a trinitrobenzene sulphonic acid (TNBS)-induced murine model of ulcerative colitis (UC) to quantify eosinophil infiltration. Our lab recently showed that the focal adhesion kinase (FAK) signaling pathway regulates eosinophil recruitment in vitro and in vivo. We used the toolset I refined to first characterize eosinophil recruitment in the TNBS colitis model and then examined the role of FAK signaling in both eosinophil recruitment and disease scores. We found that eosinophil infiltration into the colon of mice treated with in TNBS peaked at day 3 and returned to baseline by day 7, with most eosinophils being recruited to the mucosa and submucosa of the proximal colon. Inhibiting FAK decreased the number of eosinophils to baseline levels in a dose-dependent manner. Despite decreasing eosinophils to near control levels, FAK inhibition did not significantly affect disease scores such as weight loss, diarrhea or bleeding. There was, however, a slight decrease in ulceration. Utilizing a new imaging toolset, this study sheds new light on the mechanisms of eosinophil infiltration in TNBS colitis and shows that eosinophil infiltration can be disassociated from tissue damage in this model.